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Mena Mansour

Researcher at Washington University in St. Louis

Publications -  18
Citations -  1242

Mena Mansour is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Oncolytic virus & Virus. The author has an hindex of 7, co-authored 15 publications receiving 1070 citations. Previous affiliations of Mena Mansour include Icahn School of Medicine at Mount Sinai & Mount Sinai Hospital.

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Localized Oncolytic Virotherapy Overcomes Systemic Tumor Resistance to Immune Checkpoint Blockade Immunotherapy

TL;DR: In this article, the authors explored the immunotherapeutic potential of oncolytic Newcastle disease virus (NDV) and found that localized intratumoral therapy of B16 melanoma with NDV induces inflammatory responses, leading to lymphocytic infiltrates and antitumor effect in distant (nonvirally injected) tumors without distant virus spread.
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Twist is transcriptionally induced by activation of STAT3 and mediates STAT3 oncogenic function.

TL;DR: The results indicate that activated STAT3 transcriptionally induces Twist, which plays an important role in promoting migration, invasion, and anchorage-independent growth in the late stage tumor tissues.
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Oncolytic Specificity of Newcastle Disease Virus Is Mediated by Selectivity for Apoptosis-Resistant Cells

TL;DR: It is demonstrated that NDV possesses oncolytic activity in tumor cells capable of a robust type I interferon (IFN) response, suggesting that another mechanism underlies NDV's tumor specificity.
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Enhancement of Oncolytic Properties of Recombinant Newcastle Disease Virus Through Antagonism of Cellular Innate Immune Responses

TL;DR: It is demonstrated that modulation of innate immune responses by NDV results in enhancement of its oncolytic properties and warrant further investigation of this strategy in design of on colytic NDV vectors against human tumors.
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Enhancement of the Proapoptotic Properties of Newcastle Disease Virus Promotes Tumor Remission in Syngeneic Murine Cancer Models

TL;DR: The data suggest that upregulation of the proapoptotic function of NDV is a viable approach to enhance its antitumor properties and adds to the currently known, rationally based strategies to design optimized therapeutic viral vectors for the treatment of cancer.